Comparative analysis of cell surface antigens expressed by cell lines derived from human germ cell tumours

Andrews, Peter W.; Casper, Jochen; Damjanov, Ivan; Duggan-Keen, Margaret F; Giwercman, Aleksander; Hata, Junichi; Keitz, Alexander von; Looijenga, Leendert H. J.; Millán, José Luis; Oosterhuis, J. Wolter; Pera, Martin F.; Sawada, Masumi; Schmoll, H.-J.; Skakkebæk, Niels E.; Putten, Wilhelm van; Stern, Peter L.

doi:10.1002/(sici)1097-0215(19960611)66:6<806::aid-ijc17>3.0.co;2-0

Cited by 101 publications

(66 citation statements)

References 41 publications

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“…In addition, the cell lines Haz and Bos, derived from two extragonadal germ cell tumours, were studied (Sinke et al, 1994;Van Echten-Arends et al, 1995), as well as the cell line S2, of which the origin is still a matter of debate (Von Keitz et al, 1994;Andrews et al, 1996). The mesothelioma-derived cell line M25 was also investigated (Versnel et al, 1989).…”

Section: Methodsmentioning

confidence: 99%

“…The mesothelioma-derived cell line M25 was also investigated (Versnel et al, 1989). The cell lines were cultured as described before (Andrews et al, 1996). Four primary testicular seminomas and four NS-TGCTs, with the histology of pure embryonal carcinoma, pure teratoma, pure yolk sac tumour and mixed containing embryonal carcinoma, teratoma and yolk sac tumour, were investigated.…”

Section: Methodsmentioning

confidence: 99%

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Lack of Bcl10 mutations in testicular germ cell tumours and derived cell lines

et al. 1999

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Summary Aberrations within Bcl10, a gene involved in execution of apoptosis, has most recently been found in a variety of cancers, including cell lines of testicular germ cell tumours of adolescents and adults (TGCTs). To study this in more detail, we screened exons 2 and 3 of this gene for mutations in a larger series of cell lines as well as primary TGCTs by single-strand conformation polymorphism and endonuclease restriction analysis. Because no aberrations were detected, we conclude that inactivation of Bcl10 by mutation is at least far less important in the development of TGCTs than proposed.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Lack of Bcl10 mutations in testicular germ cell tumours and derived cell lines

et al. 1999

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“…Such a result would be consistent with the occurrence of partial spontaneous differentiation, and we have previously noted rather greater variability in expression of SSEA3 by NTERA2 cells, in contrast to 2102Ep, presumably reflecting the same phenomenon. 11 Following 6 days exposure to retinoic acid, the expression of both antigens was markedly diminished in TG11.nR, C7 and C10, but not in 2102Ep. At the same time, the expression of the glycolipid antigen, ganglioside GT3, detected by antibody A2B5, 15,34 was induced in TG11.nR, C7 and C10, but not in 2102Ep.…”

Section: ϫ7mentioning

confidence: 97%

“…11 A few of these EC cell lines are able to undergo extensive differentiation. For example, NTERA2, a derivative of TERA2, forms well differentiated tumors in nude mice.…”

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confidence: 99%

Hybrids of pluripotent and nullipotent human embryonal carcinoma cells: Partial retention of a pluripotent phenotype

et al. 2001

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To investigate whether the failure of human EC cells that do not differentiate is due to the loss of key differentiationpermissive functions or the acquisition of specific inhibitory functions, we tested the ability to differentiate of 2 hybrids produced between a relatively nullipotent human EC cell line, 2102Ep, and a pluripotent human EC cell line NTERA2. Both hybrids, which exhibited an EC phenotype, were able to differentiate readily in response to retinoic acid. Furthermore, 1 hybrid produced a well-differentiated xenograft tumor, which contained, like the NTERA2 tumors, glandular structures, loose mesenchymal tissues and nodules of cartilage, after injection into a SCID mouse. Thus, the failure of 2102Ep EC cells to differentiate is recessive and due to the loss of a key gene function or functions. Nevertheless, the hybrids differed from the pluripotent NTERA2 line by failing to differentiate in neurons, indicating that 2102Ep cells also had acquired a specific, dominantly-acting, inhibitory mutation specific to the neural lineage. Furthermore, the expression of collagen II by one hybrid before and after induction with retinoic suggested a propensity for spontaneous differentiation not evident in the parental NTERA2 cells. Thus, the mechanisms that restrict the differentiation capacity of the nullipotent 2102Ep line are complex and include both recessive and dominant acting factors.

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“…family were genotyped for the CϾT mutation within pseudoexon 2a of A4GALT, which allows prediction of P 1 /P 2 phenotypes (15 Generation of Cells Expressing the NOR Antigen-To further examine whether the C631G point mutation detected in the A4GALT gene is responsible for synthesis of NOR antigen, we transfected 2102Ep human teratocarcinoma cells (17,19) with vectors encoding the consensus Gb3/CD77 synthase or Gb3/ CD77 synthase with Glu at position 211 (hereafter called the Gb3/CD77 Q211E synthase). Teratocarcinoma cells were selected because they produce considerable amounts of globoside, which is a precursor of NOR (20,21). The results of our transfection experiments were evaluated by flow cytometry using an anti-NOR antibody specific to the Gal(␣1-4)GalNAc present in the NOR1 and NOR2 antigens and an anti-P1 antibody specific to the Gal(␣1-4)Gal present in the P k and P1 antigens ( Fig.…”

Section: Identification Of a Mutation Correlated With The Normentioning

confidence: 99%

A Single Point Mutation in the Gene Encoding Gb3/CD77 Synthase Causes a Rare Inherited Polyagglutination Syndrome

Suchanowska

Kaczmarek

Duk

et al. 2012

Journal of Biological Chemistry

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Background: Inheritable NOR polyagglutination is a rare phenomenon caused by the unusual Gal(␣1-4)GalNAc glycolipid epitope. Results: A point mutation, 631 CϾG, in the gene encoding Gb3/CD77 synthase causes the enzyme to synthesize both Gal(␣1-4)Gal-and Gal(␣1-4) GalNAc-moieties. Conclusion:The results pinpoint the cause of the NOR phenotype. Significance: This is the first report of an altered acceptor specificity of a glycosyltransferase caused by a point mutation.

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Comparative analysis of cell surface antigens expressed by cell lines derived from human germ cell tumours

Cited by 101 publications

References 41 publications

Lack of Bcl10 mutations in testicular germ cell tumours and derived cell lines

Lack of Bcl10 mutations in testicular germ cell tumours and derived cell lines

Hybrids of pluripotent and nullipotent human embryonal carcinoma cells: Partial retention of a pluripotent phenotype

A Single Point Mutation in the Gene Encoding Gb3/CD77 Synthase Causes a Rare Inherited Polyagglutination Syndrome

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